Recently, the [l(3)k3.13/2] gene of Drosophila melanogaster was generated in a specific genetic screen for lethals on the third chromosome. It was shown to be the Drosophila homolog of one of the mouse proteinases genes which its expression is required to cut the protein (amino acid chain) once at a specific site. The latter is always very near to the  C-terminus of the polypeptide chain thus affecting a distinct regulatory pathway. Soon it was revealed that the [l(3)k3.13/2]  gene is a tumor suppressor gene displaying malignant development of the hematopoietic organs and in some other body organs. This massive tissue overgrowth finally leads to the death of the animal as late larvae or pupae. Based on the above mentioned facts, the present investigation was designed at the aim of trying to find out the suggested functional genetic role played by this gene in Drosophila tumorigenesis. Especially, in a concert either with previously known oncogenes like Ras^v/2 or tumor suppressor genes like oho31 and Df(21) dp-38a in Drosophila.                 For this purpose, a large scale experiment including a series of different genetic crosses was carried out. The results could be   summarized as following. The analyses of the lethal phase of [l(3)k3.13/2] as well as the other strains used in this study showed that lethality always took place during late larval stage for [l(3)k3.13/2], oho-31 and Df(2L)dp-38a. In (UAS-Ras^v12) and (N14) strains, however, lethality took place during early pupal stage of Drosophila development. The lethality percentages raised up in all the (1:1) combinations of [l(3)k3.13/2] with the other four stocks used suggesting that the [l(3)k3.13/2] gene expression is required in its normal case for the function of other genes in Drosophila.                 Interestingly enough, the presence of the homozygous third chromosome [l(3)k3.13/2]/ [l(3)k3.13/2] side by side with the heterozygous second chromosome UAS-Ras^v12/N14 in the same genotype, dropped the viability to the lowest percentage at all and lethality took place during the embryonic stage (instead of being during late larval-early pupal stage), specially that was counted for y Tb⁺ larvae. This result may indicate that there is a synergistic effect of [l(3)k3.13/2] and Ras^v12 genes. Dissecting y Tb⁺ larvae revealed that their inside organs were deleteriously more affected than the control larvae. These findings confirm, at the genetic level, the idea that the tumor suppressor gene [l(3)k3.13/2] is required for the inactivation of Ras^v12 oncogene as well as for the proper genetic functions of both oho-31 and Df(2L)dp-38a tumor suppressor genes in Drosophila melanogaster. This kind of study opens a new dimension for understanding the process of tumorigenesis both in insects and in human cancer.